The concentration of Na inside vascular smooth muscle cells in an important regulator of vascular smooth muscle function, however little is known about the sarcolemmal translocation pathways which mediate Na influx. Prior studies have shown that Na flux into arterial strips is increased in several forms of experimental hypertension, but the translocation pathways involved are not known. These studies will test the hypotheses that specific transport mechanisms which mediate Na influx are present in the sarcolemma of of vascular smooth muscle cells, that an increase in the activity of one or more of these transport systems is found in mineralocorticoid induced hypertension, and that this effect of mineralocorticoids is mediated via methylation of membrane components. It is proposed to test for the presence of, and characterize four specific Na translocation pathways in sarcolemmal vesicles from canine superior mesenteric artery: 1) Na channels; 2) Na/H exchange; 3) Na/K/Cl cotransport; 4) Na/Ca exchange. The effects of aldosterone in-vitro, and DOCA-salt hypertension on the activities of these pathways will be determined. Finally, the relation between aldosterone-stimulated Na transport and the methylation of sarcolemmal phospholipids and proteins will be assessed. These studies will contribute to the fundamental understanding of Na metabolism in vascular smooth muscle cells, under normal and abnormal conditions. Such information may help establish the pathogenesis of certain hypertensive states, and lead to the development of specific therapies for these diseases.